Is microbial translocation a cause or consequence of HIV disease progression?

Journal of Infectious Diseases

Volumn 203, Issue 5, 2011, Pages 744-745

  Redd, Andrew D ^a   Gray, Ronald H ^b   Quinn, Thomas C ^a  

^a NATIONAL INSTITUTES OF HEALTH   (United States)

^b JOHNS HOPKINS BLOOMBERG SCHOOL OF PUBLIC HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ANTIRETROVIRUS AGENT; CD14 ANTIGEN; LIPOPOLYSACCHARIDE;

ACQUIRED IMMUNE DEFICIENCY SYNDROME; CROSS-SECTIONAL STUDY; DISEASE COURSE; HUMAN; HUMAN IMMUNODEFICIENCY VIRUS; HUMAN IMMUNODEFICIENCY VIRUS 1; HUMAN IMMUNODEFICIENCY VIRUS 2; HUMAN IMMUNODEFICIENCY VIRUS INFECTED PATIENT; HUMAN IMMUNODEFICIENCY VIRUS INFECTION; IMMUNE RESPONSE; LETTER; MICROBIAL TRANSLOCATION; MICROBIOLOGICAL PHENOMENA AND FUNCTIONS; MONOCYTE; NONHUMAN; PRIORITY JOURNAL; SIMIAN IMMUNODEFICIENCY VIRUS; VIRUS LOAD;

ANIMALS; BACTERIAL TRANSLOCATION; CROSS-SECTIONAL STUDIES; DISEASE PROGRESSION; HIV INFECTIONS; HIV-1; HIV-2; HUMANS; LIPOPOLYSACCHARIDES; LONGITUDINAL STUDIES;

EID: 79751508059     PISSN: 00221899     EISSN: None     Source Type: Journal    
DOI: 10.1093/infdis/jiq107     Document Type: Letter

References (15)

1. Cassol E, Malfeld S, Mahasha P, et al. Persistent microbial translocation and immune activation in HIV-1-infected South Africans receiving combination antiretroviral therapy. J Infect Dis 2010; 202:723-33.
2. Nowroozalizadeh S, Mansson F, da Silva Z, et al. Microbial translocation correlates with the severity of both HIV-1 and HIV-2 infections. J Infect Dis 2010; 201:1150-4.
3. Redd AD, Dabitao D, Bream JH, et al. Microbial translocation, the innate cytokine response, and HIV-1 disease progression in Africa. Proc Natl Acad Sci U S A 2009; 106:6718-23.
4. Redd AD, Eaton KP, Kong X, et al. C-reactive protein levels increase during HIV-1 disease progression in Rakai, Uganda, despite the absence of microbial translocation. J Acquir Immune Defic Syndr 2010; 54:556-9.
5. Gori A, Tincati C, Rizzardini G, et al. Early impairment of gut function and gut flora supporting a role for alteration of gastrointestinal mucosa in human immunodeficiency virus pathogenesis. J Clin Microbiol 2008; 46:757-8. (Pubitemid 351231331)
6. Brenchley JM, Price DA, Schacker TW, et al. Microbial translocation is a cause of systemic immune activation in chronic HIV infection. Nat Med 2006; 12:1365-71. (Pubitemid 44924494)
7. Ancuta P, Kamat A, Kunstman KJ, et al. Microbial translocation is associated with increased monocyte activation and dementia in AIDS patients. PLoS ONE 2008; 3:e2516.
8. Lester RT, Yao XD, Ball TB, et al. HIV-1 RNA dysregulates the natural TLR response to subclinical endotoxemia in Kenyan female sex-workers. PLoS One 2009; 4:e5644.
9. Wallet MA, Rodriguez CA, Yin L, et al. Microbial translocation induces persistent macrophage activation unrelated to HIV-1 levels or T-cell activation following therapy. AIDS 2010; 24:1281-90.
10. Papasavvas E, Pistilli M, Reynolds G, et al. Delayed loss of control of plasma lipopolysaccharide levels after therapy interruption in chronically HIV-1-infected patients. AIDS 2009; 23:369-75.
11. Leinert C, Stahl-Hennig C, Ecker A, et al. Microbial translocation in simian immunodeficiency virus (SIV)-infected rhesus monkeys (Macaca mulatta). J Med Primatol 2010; 39:243-51.
12. Klatt NR, Harris LD, Vinton CL, et al. Compromised gastrointestinal integrity in pigtail macaques is associated with increased microbial translocation, immune activation, and IL-17 production in the absence of SIV infection. Mucosal Immunol 2010; 3:387-98.
13. Rempel H, Sun B, Calosing C, Pillai SK, Pulliam L, et al. Interferon-alpha drives monocyte gene expression in chronic unsuppressed HIV-1 infection. AIDS 2010; 24:1415-23.
14. Ciccone EJ, Read SW, Mannon PJ, et al. Cycling of gut mucosal CD4+ T cells decreases after prolonged anti-retroviral therapy and is associated with plasma LPS levels. Mucosal Immunol 2010; 3:172-81.
15. Ferri E, Novati S, Casiraghi M, et al. Plasma levels of bacterial DNA in HIV infection: The limits of quantitative polymerase chain reaction. J Infect Dis 2010; 202:176-7; author reply 178.